MedChemExpress -Model Tyroserleutide hydrochloride -852982-42-4

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Tyroserleutide hydrochloride is a tripeptide isolated from the degradation products of porcine spleen with antitumor activity. Tyroserleutide hydrochloride can upregulate the expression of the tumor suppressor gene PTEN and inhibit the activity of AKT and PDK1. Tyroserleutide hydrochloride inhibits tumor cell proliferation and MDM2 phosphorylation by inhibiting the PI3K/AKT pathway, and also upregulates P21, P27, P53, and induces mitochondrial damage and cell apoptosis[1][2][3].
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Tyroserleutide hydrochloride

MCE China:Tyroserleutide hydrochloride

Brand:MedChemExpress (MCE)

Cat. No.HY-106263B

CAS:852982-42-4

Purity:99.98%

Storage:Sealed storage, away from moisture and light, under nitrogen Powder -80°C 2 years -20°C 1 year *In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light, under nitrogen)

Shipping:Room temperature in continental US; may vary elsewhere.

Description:Tyroserleutide hydrochloride is a tripeptide isolated from the degradation products of porcine spleen with antitumor activity. Tyroserleutide hydrochloride can upregulate the expression of the tumor suppressor gene PTEN and inhibit the activity of AKT and PDK1. Tyroserleutide hydrochloride inhibits tumor cell proliferation and MDM2 phosphorylation by inhibiting the PI3K/AKT pathway, and also upregulates P21, P27, P53, and induces mitochondrial damage and cell apoptosis.

In Vitro:Tyroserleutide (YSL) exhibits immuno-modulating effects, such as enhancing concanavalin (ConA) induced proliferation of mouse spleen lymphocytes, phagocytosis of mouse peritoneal macrophages, and the activity of natural killer (NK) cells[1]. Tyroserleutide (YSL), an immunologically therapeutic tripeptide, can promote hepatocarcinoma cell (H22) apoptosis through downregulating Bcl-2 and cyclin D1 expression[2]. Tyroserleutide is an ideal choice for inducing apoptosis of liver tumor cells[2]. Tyroserleutide inhibits tumor growth and does not cause severe toxicities in the major organs. Tyroserleutide can inhibit tumor cell migration[2].

In Vivo:Tyroserleutide (10-80 μg/kg; injection (i.p.) one time every day until mice are dead) displays obvious anti-tumor activity. Tyroserleutide significantly prolongs the survival time of the murine H22 implanted mice[1].

IC50 & Target:Antitumor tripeptide[1][2] In Vitro Tyroserleutide (YSL) exhibits immuno-modulating effects, such as enhancing concanavalin (ConA) induced proliferation of mouse spleen lymphocytes, phagocytosis of mouse peritoneal macrophages, and the activity of natural killer (NK) cells[1]. Tyroserleutide (YSL), an immunologically therapeutic tripeptide, can promote hepatocarcinoma cell (H22) apoptosis through downregulating Bcl-2 and cyclin D1 expression[2]. Tyroserleutide is an ideal choice for inducing apoptosis of liver tumor cells[2]. Tyroserleutide inhibits tumor growth and does not cause severe toxicities in the major organs. Tyroserleutide can inhibit tumor cell migration[2]. MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. 0 --> Tyroserleutide hydrochloride Related Antibodies

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References:

[1]. Fu Z, et al. Effects of Tyroserleutide on phosphatidylinositol 3'-kinase/AKT pathway in human hepatocellular carcinoma cell. J Drug Target. 2014 Feb;22(2):146-55.  [Content Brief]

[2]. Wang C, et al. Studies on the large scale synthesis and anti-tumor activity of YSL. Prep Biochem Biotechnol. 2003 Aug;33(3):189-95.  [Content Brief]

[3]. Liang P, et al. pH-Triggered Conformational Change of Antp-Based Drug Delivery Platform for Tumor Treatment with Combined Photothermal Therapy and Chemotherapy. Adv Healthc Mater. 2019 Aug;8(15):e1900306.  [Content Brief]

[4]. Che X, Lu R, Fu Z, et al. Therapeutic effects of tyroserleutide on lung metastasis of human hepatocellular carcinoma SK-HEP-1 and its mechanism affecting ICAM-1 and MMP-2 and -9. Drug Des Devel Ther. 2018;12:3357-3368.  [Content Brief]

[5]. Yao Z, Qiu S, Wang L, et al. Tripeptide tyroserleutide enhances the antitumor effects of macrophages and stimulates macrophage secretion of IL-1beta, TNF-alpha, and NO in vitro. Cancer Immunol Immunother. 2006;55(1):56-60.  [Content Brief]

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